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IRES-Dependent Translational Control during Virus-Induced Endoplasmic Reticulum Stress and Apoptosis

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      Abstract

      Many virus infections and stresses can induce endoplasmic reticulum (ER) stress response, a host self-defense mechanism against viral invasion and stress. During this event, viral and cellular gene expression is actively regulated and often encounters a switching of the translation initiation from cap-dependent to internal ribosome-entry sites (IRES)-dependent. This switching is largely dependent on the mRNA structure of the 5′ untranslated region (5′ UTR) and on the particular stress stimuli. Picornaviruses and some other viruses contain IRESs within their 5′ UTR of viral genome and employ an IRES-driven mechanism for translation initiation. Recently, a growing number of cellular genes involved in growth control, cell cycle progression and apoptosis were also found to contain one or more IRES within their long highly structured 5′ UTRs. These genes initiate translation usually by a cap-dependent mechanism under normal physiological conditions; however, in certain environments, such as infection, starvation, and heat shock they shift translation initiation to an IRES-dependent modality. Although the molecular mechanism is not entirely understood, a number of studies have revealed that several cellular biochemical processes are responsible for the switching of translation initiation to IRES-dependent. These include the cleavage of translation initiation factors by viral and/or host proteases, phosphorylation (inactivation) of host factors for translation initiation, overproduction of homologous proteins of cap-binding protein eukaryotic initiation factors (eIF)4E, suppression of cap-binding protein eIF4E expression by specific microRNA, activation of enzymes for mRNA decapping, as well as others. Here, we summarize the recent advances in our understanding of the molecular mechanisms for the switching of translation initiation, particularly for the proteins involved in cell survival and apoptosis in the ER stress pathways during viral infections.

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      Most cited references 161

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      miRBase: tools for microRNA genomics

      miRBase is the central online repository for microRNA (miRNA) nomenclature, sequence data, annotation and target prediction. The current release (10.0) contains 5071 miRNA loci from 58 species, expressing 5922 distinct mature miRNA sequences: a growth of over 2000 sequences in the past 2 years. miRBase provides a range of data to facilitate studies of miRNA genomics: all miRNAs are mapped to their genomic coordinates. Clusters of miRNA sequences in the genome are highlighted, and can be defined and retrieved with any inter-miRNA distance. The overlap of miRNA sequences with annotated transcripts, both protein- and non-coding, are described. Finally, graphical views of the locations of a wide range of genomic features in model organisms allow for the first time the prediction of the likely boundaries of many miRNA primary transcripts. miRBase is available at http://microrna.sanger.ac.uk/.
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        Regulation of translation initiation in eukaryotes: mechanisms and biological targets.

        Translational control in eukaryotic cells is critical for gene regulation during nutrient deprivation and stress, development and differentiation, nervous system function, aging, and disease. We describe recent advances in our understanding of the molecular structures and biochemical functions of the translation initiation machinery and summarize key strategies that mediate general or gene-specific translational control, particularly in mammalian systems.
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          Regulation of mRNA translation and stability by microRNAs.

          MicroRNAs (miRNAs) are small noncoding RNAs that extensively regulate gene expression in animals, plants, and protozoa. miRNAs function posttranscriptionally by usually base-pairing to the mRNA 3'-untranslated regions to repress protein synthesis by mechanisms that are not fully understood. In this review, we describe principles of miRNA-mRNA interactions and proteins that interact with miRNAs and function in miRNA-mediated repression. We discuss the multiple, often contradictory, mechanisms that miRNAs have been reported to use, which cause translational repression and mRNA decay. We also address the issue of cellular localization of miRNA-mediated events and a role for RNA-binding proteins in activation or relief of miRNA repression.
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            Author and article information

            Affiliations
            1simpleDepartment of Pathology and Laboratory Medicine, The Institute for Heart and Lung Health, St. Paul’s Hospital, University of British Columbia Vancouver, BC, Canada
            Author notes

            Edited by: Akio Adachi, The University of Tokushima Graduate School, Japan

            Reviewed by: Chris Sullivan, University of Texas at Austin, USA; Dahlene N. Fusco, Massachusetts General Hospital, USA

            *Correspondence: Decheng Yang, The James Hogg Research Center, St. Paul’s Hospital, University of British Columbia, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6. e-mail: decheng.yang@ 123456hli.ubc.ca

            This article was submitted to Frontiers in Virology, a specialty of Frontiers in Microbiology.

            Journal
            Front Microbiol
            Front Microbiol
            Front. Microbio.
            Frontiers in Microbiology
            Frontiers Research Foundation
            1664-302X
            19 March 2012
            2012
            : 3
            3307021
            22461781
            10.3389/fmicb.2012.00092
            Copyright © 2012 Hanson, Zhang, Hemida, Ye, Qiu and Yang.

            This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

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            Figures: 2, Tables: 0, Equations: 0, References: 160, Pages: 16, Words: 15661
            Categories
            Microbiology
            Review Article

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